Figure 7.
Figure 7. Inhibition of NETs attenuates intravascular coagulation and end-organ damage in sepsis. (A) Representative resonance-scanning confocal intravital microscopy images of the lung microvasculature of endotoxemic mice showing intravascular thrombin activity (green), NETs (blue, AF647 anti-NE), and neutrophils (red, PE-anti-Gr1). Microvascular thrombin probe fluorescence was quantified in the lung microvasculature in response to intratracheal LPS (B), and liver microvasculature in response to i.p. E coli (C) in PAD+/+ and PAD4−/− mice. (D) Plasma TAT levels were quantified in PAD4+/+ and PAD4−/− mice 6 hours after IV S aureus infection. Plasma levels of (E) PAI-1, (F) ALT, and (G) creatinine were measured in PAD4+/+ and PAD4−/− mice with E coli peritonitis (24 hours postinfection). Data are represented as mean ± SEM. **P < .01, *P < .05; N = 5-10 mice per group.

Inhibition of NETs attenuates intravascular coagulation and end-organ damage in sepsis. (A) Representative resonance-scanning confocal intravital microscopy images of the lung microvasculature of endotoxemic mice showing intravascular thrombin activity (green), NETs (blue, AF647 anti-NE), and neutrophils (red, PE-anti-Gr1). Microvascular thrombin probe fluorescence was quantified in the lung microvasculature in response to intratracheal LPS (B), and liver microvasculature in response to i.p. E coli (C) in PAD+/+ and PAD4−/− mice. (D) Plasma TAT levels were quantified in PAD4+/+ and PAD4−/− mice 6 hours after IV S aureus infection. Plasma levels of (E) PAI-1, (F) ALT, and (G) creatinine were measured in PAD4+/+ and PAD4−/− mice with E coli peritonitis (24 hours postinfection). Data are represented as mean ± SEM. **P < .01, *P < .05; N = 5-10 mice per group.

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